Etomoxir is an irreversible inhibitor of carnitine palmitoyltransferase 1a (CPT-1a) (IC50=5-20 nM). Etomoxir inhibits fatty acid oxidation by inhibiting CPT-1a, inhibits palmitate oxidation, has an inhibitory effect on adenine nucleotide translocase, and can inhibit macrophage polarization by disrupting CoA homeostasis.

faTT cellsy acid (Hepatocyte cells,human):0.1 μM, faTT cellsy acid (Hepatocyte cells,rat):10 μM, faTT cellsy acid (Hepatocyte cells,guinea pig):1 μM, KB cells (human):2.76 μM

METHODS: A2780/PTX cells were treated with Etomoxir (1, 10, 100, 1000, 10000, 100000 nM) and paclitaxel (1, 10, 100, 1000, 10000, 100000 nM) for 48 hours, and the growth inhibition of the cells was detected by the CCK-8 method.
RESULTS: The IC50 value of Etomoxir decreased from 1589.5 ± 62.5 nM to 817.4 ± 79.7 nM. [1]

METHODS: To study the inhibition of cardiac CPT-I activity by Etomoxir, rats were injected with Etomoxir daily for 8 consecutive days at a dose of 20 mg/kg.
RESULTS: Rats treated with Etomoxir showed a 44% reduction in cardiac CPT-I activity.
METHODS: To study the effects of Etomoxir on blood glucose levels, weight gain, hind limb muscle mass, heart mass and liver mass, Lewis rats were treated with 20 mg/kgEtomoxir for 8 days.
RESULTS: Treating Lewis rats with Etomoxir for 8 days did not change the blood glucose level, did not affect general growth characteristics such as weight gain, nor did it affect the muscle mass of the hind limbs. However, both the heart mass and liver mass increased significantly by 11%. [2]